ABSTRACT
In rkcknt ekars,thk incidknck of childhood obksite has also incrkaskd ekar be ekar as pkoplk＇s living standards ckkp improving. Ovkr-accumulation of adiposk tissuk in childrkn with obksite not onle affkcts growth and dk-vklopmknt,but also incrkasks thk risc of ckrtain rklatkd mktabolic diskasks such as insulin rksistanck and tepk 2 diabk-tks. It has bkkn rkcognizkd that adiposk tissuk is thk main sitk of obksite-induckd kndoplasmic rkticulum strkss and plaes an important rolk in thk dkvklopmknt of insulin rksistanck and tepk 2 diabktks. Ls thk largkst human kndocrink or-gan,adiposk tissuk will bk considkrkd as a cke targkt for thk trkatmknt of obksite-rklatkd mktabolic diskasks in chil-drkn. Now,thk mkchanism of insulin rksistanck and tepk 2 diabktks in childrkn with obksite causkd be kndoplasmic rk-ticulum strkss in adiposk tissuk wkrk brikfle rkvikwkd,and thk rolk of adiposk tissuk in thk dkvklopmknt of obksite-associatkd tepk 2 diabktks was dkkple undkrstandkd. It is bknkficial for pkoplk to activkle promotk thk prkvkntion and trkatmknt of childhood obksite and providk nkw idkas for clinical trkatmknt of child-rklatkd mktabolic diskasks.
ABSTRACT
The aim of the current investigations was to examine the effects of a low-carbohydrate high-fat diet (LC-HFD) on body weight, body composition, growth hormone (GH), IGF-I, and body weight regain after stopping the dietary intervention and returning the diet back to standard laboratory chow (CH). In study one, both adolescent and mature male Wistar rats were maintained on either an isocaloric LC-HFD or CH for 16 days before having their diet switched. In study two, mature rats were maintained on either LC-HFD or CH for 16 days to determine the effects of the LC-HFD on fat pad weight. LC-HFD leads to body weight loss in mature rats (P < 0.01) and lack of body weight gain in adolescent rats (P < 0.01). Despite less body weight, increased body fat was observed in rats maintained on LC-HFD (P < 0.05). Leptin concentrations were higher (P < 0.05), and IGF-I (P < 0.01) concentrations were reduced in the LC-HFD rats. When the diet was returned to CH following LC-HFD, body weight regain was above and beyond that which was lost (P < 0.01). The LC-HFD resulted in increased body fat and had a negative effect upon both GH and IGF-I concentrations, which might have implications for the accretion and maintenance of lean body mass (LBM), normal growth rate and overall metabolic health. Moreover, when the LC-HFD ceases and a high-carbohydrate diet follows, more body weight is regained as compared to when the LC-HFD is consumed, in the absence of increased energy intake.
Subject(s)
Body Weight/drug effects , Diet, Carbohydrate-Restricted , Dietary Fats/pharmacology , Energy Metabolism/drug effects , Homeostasis/drug effects , Weight Gain/drug effects , Animals , Blood Glucose/metabolism , Body Composition/drug effects , Body Composition/physiology , Body Weight/physiology , Energy Metabolism/physiology , Growth Hormone/blood , Homeostasis/physiology , Insulin/blood , Insulin-Like Growth Factor I/metabolism , Male , Rats , Rats, Wistar , Serum Albumin/metabolism , Weight Gain/physiologyABSTRACT
Objective To investigate the expression and effect of elastin in full-term rats with hyperoxia induced by chronic lung diseases. Methods One hundred and forty-four full-term rats are randomly exposed to hyperoxia (hyperoxia group)and room air(room air group).Chronic lung disease(CLD)is induced by hyperoxia exposure. Gomori's stain for elastic fibers and in situ hybridization methods were used to detect the expressions of secondary crest and tropoelastin mRNA on the 1st,3 rd, 7th, 10th,14th and 21st days after exposure. Results The expressions of secondary crest decreased significantly in hyperoxia group, compared with room air group on the 3rd to 14th days(P＜0.05).The expressions of tropoelastin mRNA decreased significantly in hypemxia group, compared with room air group on the 3rd to 10th days (P＜0.05),otherwise increased significantly from the 14th to 21 st days(P＜0.05). Hyperoxia exposure can delay the peak of tropoelastin mRNA. Conclusion Elastin is involved in the inhibition of alveolarization and lung fibrosis in the development of CLD.
